Eligibility criteria for participation in mental health jail diversion programs often specify that, to be diverted, a candidate must not pose a level of threat to public safety that cannot be managed in the community. Risk assessment tools were developed to increase consistency and accuracy in estimates of threat to public safety. Consequently, risk assessment tools are being used in many jurisdictions to inform decisions regarding an individual’s appropriateness and eligibility for mental health jail diversion and the strategies that may be successful in mitigating risk in this context. However, their use is not without controversy. Questions have been raised regarding the validity and equity of their estimates, as well as the impact of their use on criminal justice outcomes. The purpose of this review is to provide an overview of the science and practice of risk assessment to inform decisions and case planning in the context of mental health jail diversion programs. Our specific aims include: (1) to describe the process and components of risk assessment, including differentiating between different approaches to risk assessment, and (2) to consider the use of risk assessment tools in mental health jail diversion programs. We anchor this review in relevant theory and extant research, noting current controversies or debates and areas for future research. Overall, there is strong theoretical justification and empirical evidence from other criminal justice contexts; however, the body of research on the use of risk assessment tools in mental health jail diversion programs, although promising, is relatively nascent.

Impulsive violence may be the behavioral consequence of inefficient information processing within specific neuronal networks. Analogous to the hypothetical pathophysiology of addiction, maladaptations within reward pathways may shift goal-directed behaviors to impulsive reactions and then to compulsive habits, in order to create impulsive violence.

Whose job is it to discover and manage patients' sexual concerns? If you believe that you have a role to play, just what is that role and how will you perform it? Sexual disorders are common, yet infrequently diagnosed. A willingness to inquire about sexual function is the most critical diagnostic step for clinicians. Once a problem is discovered, a systematic diagnostic process can uncover etiologic organic and psychogenic factors using customary diagnostic tools, including taking a psychosexual and medical history, comprehensive and focused physical examinations, psychological assessment instruments, laboratory tests, and special procedures.

Twin, family, and adoption studies indicate that genetic factors play a major role in predisposition to schizophrenia. To date, molecular genetic studies have implicated many different chromosomal locations for the disorder. However, no one site replicates across the majority of investigations. This creates an impasse in the study of schizophrenia genetics, because of the large number of chromosomal sites that require further detailed research. It is difficult to plan to move ahead with expensive and labor-intensive research in an attempt to determine the etiologie genetic factor, when any given site proves to be only weakly positive. Therefore, the use of a hypothesis-driven approach may be cost effective, and may ultimately have more power to detect etiologie genes. Several lines of evidence suggest that a neurodevelopmental defect may play an important role in the etiology of this disorder. Neurodevelopment is a complex process in which genetic and nongenetic factors may interact to create the mature differentiated neuron, with its particular network of synaptic connections. A reasonable chance exists that polymorphisms of the genes that control normal development of the central nervous system (CNS) may produce a slightly altered trajectory of brain development, predisposing individuals to schizophrenia. This assumption has led geneticists to begin to study neurodevelopmental genes in schizophrenia subjects. This article reviews and discusses genetic studies of some developmental genes in schizophrenia. Genetic association and linkage studies of neurotrophic factors (brain-derived neurotrophic factor, or BDNF, and neurotrophin-3, or NT-3), neuronal cell adhesion molecule (NCAM), synapsin, and synaptosome-associated protein with a mass of 25 kd (SNAP-25) have proven to be of most interest.

This report describes the case of a young man with a large calcification in the right thalamus that was first diagnosed at 9 years of age. Case history reveals specific eating rituals and other obsessive-compulsive personality traits during the patient's childhood and adolescence, fulfilling diagnostic criteria of obsessive-compulsive personality disorder. After a critical life event the patient develops anorexia nervosa. We suggest that our case and further literature provide evidence for an involvement of specific thalamic structures, such as the dorsomedial nucleus, in the development of anorexia nervosa. Furthermore, the treatment of the patient by a combined psychotherapeutic and pharmacotherapeutic approach is described. We focus on the beneficial effect of the atypical antipsychotic olanzapine, which can induce weight gain by an increase of leptin levels.

Trichotillomania (TTM, repetitive hair pulling) is a complex underdiagnosed syndrome that often causes considerable psychological distress and physical disfigurement. Although many aspects of hair pulling bear similarity to compulsions of obsessive-compulsive disorder (OCD), TTM lacks obsessions associated with OCD. The phenomenology of TTM also is similar to tics in Tourette Syndrome (TS) and overlaps with TS in both limited structural neuroimaging data and in terms of treatment response to pharmacotherapy with dopamine antagonists.

In order to study potential comorbid relationships between TTM, TS, and OCD, a total of 61 patients with either TS, OCD, or OCD comorbid with TS were assessed using structured interviews as part of a phenomenological study of these groups. Post hoc analyses indicated significantly higher proportions of hair pulling in those subjects with OCD comorbid with TS compared to subjects with either OCD or TS alone.

These data, in conjunction with clinical phenomenology, neuroimaging results, and response to pharmacotherapy suggest the possibility that some forms of TTM may be more closely related to tic disorders than OCD. Futher research is needed to clarify and confirm these observations of putative relationships between TTM and TS and potential treatment implications.

We appear to be on the brink of a new epoch of treatment for Alzheimer's disease. Compelling evidence suggests that Aβ42 secretion is the triggering event in the pathogenesis of Alzheimer's disease, and that tau aggregation may be an important secondary event linked to neurodegeneration. Prophylactic administration of anti-amyloid agents designed to prevent Aβ accumulation in persons with subclinical disease is likely to be more effective than therapeutic interventions in established Alzheimer's disease. Drug development programs in Alzheimer's disease focus primarily on agents with anti-amyloid disease-modifying properties, and many different pharmacologic approaches to reducing amyloid pathology and tauopathy are being studied. Classes of therapeutic modalities currently in advanced-stage clinical trial testing include forms of immunotherapy (activeβ-amyloid immunoconjugate and human intravenous immunoglobulin), a γ-secretase inhibitor, the selective Aβ42-lowering agent R-flurbiprofen, and the anti-aggregation agent tramiprosate. Non-traditional dementia therapies such as the HMG-CoA reductase inhibitors (statins), valproate, and lithium are now being assessed for clinical benefit as anti-amyloid disease-modifying treatments. Positive findings of efficacy and safety from clinical studies are necessary but not sufficient to demonstrate that a drug has disease-modifying properties. Definitive proof of disease-modification requires evidence from validated animal models of Alzheimer's disease; rigorously controlled clinical trials showing a significantly improved, stabilized, or slowed rate of decline in cognitive and global function compared to placebo; and prospectively obtained evidence from surrogate biomarkers that the treatment resulted in measurable biological changes associated with the underlying disease process.

Systematic investigations indicate that some of the recognized psychiatric disorders can be identified among those with mental retardation due to chromosomal abnormalities. We report a psychotic patient with mild mental retardation (intelligence quotient: 68) and minor anomalies that had a chromosomal aberration not previously described in a psychotic patient. Our patient highlights the importance of the cytogenetic study in psychiatric patients with comorbid mental retardation or minor anomalies. In addition, her psychosis symptoms may be helpful to propose a new candidate gene for psychosis.

Historically, drugs that increase central cholinergic transmission have primarily been investigated for relieving cognitive symptoms in mild-to-moderate Alzheimer's disease. These efforts have led to the somewhat unexpected findings that cholinergic therapy has a beneficial effect on selected neuropsychiatric symptoms in AD across disease stages. In Parkinson's disease with dementia and dementia with Lewy bodies, cholinergic deficits are more severe than in AD, and there is emerging evidence that cholinesterase inhibitors are efficacious in treating core symptoms of attentional disturbance and psychosis. Recent data also suggest a rational basis for cholinergic therapy in vascular dementia. The cognitive and neuropsychiatric effects of cholinergic therapy observed in AD and other dementias form the crux of an integrative model of cholinergic therapeutic efficacy that encompasses the diverse central nervous system actions of acetylcholine and its complementary interactions with central monoamine transmitters. This heuristic framework highlights the broader therapeutic potential of cholinergic therapy for symptom-based indications in other neuropsychiatric disorders.

Bullying is an omnipresent problem with high prevalence in children and adolescents. There are many antibullying state laws and practices in place however its real level impact is ambiguous at best. We studied the prevalence of bullying in the United States, examine the practices, laws, and interventions in place to prevent bullying and its real-life impact. Various studies have reported that the ground-level change brought about by these policies and programs varies and is not quite significant. The effectiveness of existing policies and legislations remains unclear and measurable objective change or impact is not yet observed. Therefore, a rethink of the strategies is needed. The focus must be on community-level programs and interventions with inclusive approaches involving all the stakeholders are critical for addressing this menace.

The prevalence of autism spectrum disorder (ASD) continues to see a trend upward with a noticeable increase to 1 in 36 children less than 8 years of age in the recent MMWR. There are many factors linked to the substantially increased burden of seeking mental health services, and clinically these individuals are likely to present for impairments associated with co-occurring conditions. The advances in cutting-edge research and the understanding of co-occurring conditions in addition to psychosocial interventions have provided a window of opportunity for psychopharmacological interventions given the limited availability of therapeutics for core symptomatology. The off-label psychopharmacological treatments for these co-occurring conditions are central to clinical practice. However, the scattered evidence remains an impediment for practitioners to systematically utilize these options. The review collates the crucial scientific literature to provide stepwise treatment alternatives for individuals with ASD; with an aim to lead practitioners in making informed and shared decisions. There are many questions about the safety and tolerability of off-label medications; however, it is considered the best practice to utilize the available empirical data in providing psychoeducation for patients, families, and caregivers. The review also covers experimental medications and theoretical underpinnings to enhance further experimental studies. In summary, amidst the growing clinical needs for individuals with ASD and the lack of approved clinical treatments, the review addresses these gaps with a practical guide to appraise the risk and benefits of off-label medications.